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218 Cards in this Set

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Clinical Interpretation:
there is a variation of the R
to R interval, with the heart
rate speeding up and
slowing down (compare
heart rate in V1, V2 and V3
with the heart rate in V4,
V5, and V6)
• Summary: Normal EKG with
sinus arrhythmia (variation
of heart rate related to
respiration)
ekg
• The EKG shows:
– Narrow‐complex tachycardia, with
rate of approximately 200 bpm
– No P waves are visible
– Normal axis
– Normal QRS complexes, ST segment
and T waves
• Clinical interpretation:
– Supraventricular tachycardia, and,
since no P waves are visible, this is a
junctional tachycardia
• What to do
– Junctional tachycardia is the most
common form of paroxysmal
tachycardia in young people
– Try intravenous injection of
adenosine
– If unsuccessful: verapamil (5‐10 mg)
in bolus IV
– If unsuccessful: cardioversion
what does this ekg show you AND what should you?
• Clinical Interpretation: tall R
waves in V1 and reduced R
wave progression in the
precordial leads. Right axis
deviation with mean QRS
vector of approximately +120
degrees
• Summary: Right axis deviation
with suspicion of right
ventricular hypertrophy.
Consider execution of
echocardiogram
type ekg?
• Clinical Interpretation:
Vertical heart (mean
QRS vector of
approximately +90
degrees)
• Summary: Normal EKG
(vertical heart is a
normal variant)
type ekg?
• Clinical
Interpretation: R‐R’
aspect in V5 and V6
• Summary: Left
bundle branch block
type ekg?
• Clinical
Interpretation: ST
segment elevation in
LII, LIII and AVF
(inferior leads)
• Summary: Acute
inferior myocardial
infarction
type ekg?
• Clinical Interpretation:
Positivity of Socolow
and Lewis indexes with
ST segment depression
in V5 and V6
• Summary: Left
ventricular
hypertrophy, with
ventricular strain
ekg?
• Clinical Interpretation:
PR interval >0.2 sec; RR’
aspect in V1 and V2;
right axis deviation
• Summary: 1st degree AV
block; Right bundle
branch block; right axis
deviation
ekg?
• Clinical Interpretation:
Deep Q waves in LII, LIII
and AVF; ST segment
elevation in V1 through
V6
• Summary: Old inferior
myocardial infarction;
acute anterior
myocardial infarction
ekg?
• The EKG shows:
– Broad‐complex tachycardia, rate
about 250 per min
– Regular QRS complexes
– QRS duration 200ms
• Clinical Interpretation:
– In the context of acute
myocardial infarction a
broad‐complex tachycardia
should be considered to be
ventricular
• What to do
– In case of severe
hemodynamic impairment,
immediate cardioversion
• Summary
– Ventricular tachycardia
ekg?
• The EKG shows:
– Atrial fibrillation
– Ventricular rate: 75‐200 bpm (need to calculate mean ventricular rate by means of a long LII o V1 strip)
– Normal axis
– Normal QRS complexes
– Downsloping ST segment depression, in V5 and V6
• Clinical Interpretation:
– The heart rate is no adequately controlled. ST depression, in absence
of hypertrophy and ischemia, suggest that the patient is taking digossin
• What to do
– Check cardiac function by
echocardiogram
– Check serum levels of digossin and, if necessary, increase the dose.
– Consider cardioversion to reestablish sinus rhythm, after adequate anticoagulant therapy
ekg?
• The EKG shows:
– Sinus tachycardia
– Horizontal heart
– Normal QRS complexes
– ST segment depression:
horizontal in V3‐V4, ownsloping in LI, AVL, V5‐V6
• Clinical interpretation
– Anterior and lateral ischemia, without evidence of infarction.
Given the history, the diagnosis is unstable angina
• What to do
– Give aspirin, and intravenous heparin and nitrates
– Also intravenous beta‐ blockade can help!
ekg? what do you do?
• The EKG shows:
– Sinus rhythm
– Normal heart rate
– Normal axis
– ST elevation in inferiro leads
– Tall R wave in V1‐V2, with ST depression and T wave
inversion in V1‐V3
• Clinical interpretation
– Acute inferior and posterior
myocardial infarction
• What to do
– Immediate revascularization
ekg?
• The EKG shows:
– Sinus rhythm
– Normal axis
– Q waves in inferior leads
– Marked ST elevation in
Leads V1‐V6
• Clinical interpretation
– Old inferior infarction,
and acute anterior MI
• What to do
– Revascularize asap
ekg?
• The EKG shows:
– Sinus Rhythm
– Normal axis
– Normal QRS complexes
– Marked (about 8 mm)
horizontal ST segment
depression in leads V2‐V4,
and downsloping ST segment
depression in the lateral leads
• Clinical interpretation
– Severe antero‐lateral
ischemia (unstable angina)
• What to do
– Aspirin, heparin, nitrates iv
ekg? and what do you do?
1. major change: elevated pressure in LA and pul vasc.

2. complicated with RV hypertrophy/failure due to pul htn
What hemodynamic change occurs here?
A fib, tx with cardiac glycosides (digoxin)dec av conduction and depress sa node
what ekg change is associated with this? How is it treated
1. dec vent compliance, interstial collagen

2. possible dec contractility chronically, myosin ATPase activity depressed

3. perfusion deficit, reduced coronary reserves (volume>capillary)

4. less efficient energy utilization sarcomere mass > mitochondrial mass
What are the adverse consequenses of this?
MS with dilated LA

1. with dilated LA, mural thrombi and emboli can develop

2. acute pulmonary congestion results in alveolar hemosiderin deposits

3. pulmonary venous htn may result in thickening of pulmonary vessels causing perminant inc in pul vasc resistance
What secondary adaptive pathology and their sequelae can occur here?
1. diffuse fiberous thinkening leading to rigidity of both leaflets

2. commissural fusion **DX of rheumatic etiology

3. chordal fusion, thickening, shortening**DX of rheumatic etiology

4. calcification
What are the primary pathologies here?
1. congenital bicuspid

2. • increased systolic pressure (pressure overload)
• LV hypertrophy; concentric type, normal chamber volume
• LV compliance decreases (becomes harder to fill)
• preload must increase to maintain constant output
• LA hypertrophy
1. What is the pathology here?

2. Name one hemodynamic change that can occur here?
1. as 2nd to chronic rheumatic heart disease

2. • increased systolic pressure (pressure
overload)
• LV hypertrophy; concentric type, normal chamber volume
• LV compliance decreases (becomes harder to fill)
• preload must increase to maintain constant output
• LA hypertrophy
1. What is the cause of this?

2. Name one hemodynamic change that occurs.
pt > 70 yo, this is senile calcific aortic stenosis

clinical presentation:
– Dyspnea
– Syncope
– Angina
– Sudden death
What patient population would this be seen in? and how would they present
• Pulsus parvus et tardus
(decreased volume & slow
upstroke pulse)

• Powerful, sustained apical
systolic impulse S4

• Early ejection sound (click)
that diminishes with age in
congenital AS

• Diamond shaped systolic
murmur, peaking later in
systole and lasting longer
with severe AS.

• Single S2
What cardiac findings occur with this lesion?
1. loud S1

2. opening snap during diastole

3. mid diastolic murmur

4. presystolic accentuation (PSA) due to atrial contraction which is absent with A Fib
32 yo female pt presents with sob and hoarse voice starting 6 mo with past history of fever when younger. What cardiac findings will be seen with this pt?
1. surgery when pt sypmtomatic with transaortic gradient > 50 mm hg

2. balloon valvuloplasty pallitive for elderly pt
What are 2 txmt options for this pt?
This is a floppy mitral valve.

floppy valve: myxoid egeneration causing thickened but floppy leaflets

rheumatic: diffuse fibrous thickening of valve leaflets at the margins of closure causing leaflet retraction and poor closing. Chordal fusion/thickening is rare.
What cardiac lesions can cause this?
This is mitral regurg due to acute bacterial endocarditis

• over time, eccentric LV hypertrophy

• the regurgitant volume is pumped into a low pressure chamber (the LA) and
therefore, cardiac work is not greatly increased

• the chronic condition is well tolerated
What hemodynamic alteration and adaptation occurs here?
Thisis an acute bacterial endocarditis which causes MR.

In Chronic MR, PE findings include:

1. hyperdynamic lateral displaced apical impulse

2. parasternal lift

3. S1 often obscured by holosystolic blowing apical murmur that may radiate to axilla

4. loud S3 sound
What physical exam features are seen with a chronic case?
this is a mitral valve prolapse which presents as midsystolic click and later systolic murmur
how does this present on physical exam?
rheumatic, endocarditis,
calcific/degenerative, bicuspid
What are valvular causes of this?
dilated root in Marfan's syndrome

root pathologies include:

->idiopathic, syphilis, ankylosing spondylitis (inflammation), dissection, trauma

also

-abnormal collagen (marfan's synderome)

-calcifiation (collagen vascular disease)
What root pathologies cause this?
Polyarteritis Nodosa (PAN)

-transmural acute necrotizing inflamation of med sized vessles

-can produce irregular aneurysmal dilation, nodularity and vascular obstruction and possible infact in kidney, heart, bowels and skin but NOT LUNG AND AORTA
What clinical finding can be associated with this?
Polyarteritis Nodosa, bc transmural acute necrotizing inflamation of med sized vessels possibly causing vascular obstuction inc chance of infact from thrombi
what condition would lead to this?
This is from a pt with PAN who suffered MI 24 - 48 hrs prior, notice pmn infiltrate, edema and cell structure loss
What is the cause of change in tissue on the left?
This is Wegener's Granulomatosis

1. necrotizing granulomas of the upper and/or lower respiratior tract

2. necrotizing or granulmatous vasculitis of small arteriies and veins, usually lungs

3. necrotizing glomerulonephritis, C-ANCA presents 95% of time

txmt: respond to steroid
What triad is associated with this condition?

txmt?
corticosteriod
Pt presents with pain when chewing, has blindness in eye on same side, muscle and joint pt. Labs show inc in erthrocyte sedimentation rate. How should this pt be tx?
This is temporal arteritis or giant cell arteritis

->segmental acute and chronic, granulatomatous vascularitis involving often large areties of head particularly carotid artery branches
what condition has this histological finding and what vessels are involved?
Takayasu's arteritis also known as pulseless disease

-granulatomatous large vessel vasculitis involving aortic arch vessels
Pt comes in with complaint of cold and numb fingers. Physical finding show absence of upper extremity pulse. What vascular changes are associated with this pt condition?
child presents to ED with intenstly crying with high fever, parents have tried to give pt tylenol and advil to dec temp with no result. You notice that the pt also has red swollen palms and soles of his feet. The child's eyes are also irritated and red eyes. What immediate concern do you have for this pt?
MI due to thrombis. This child is suffering from Kawaski disease which is necrotizing mid sized vessel vasculitis involving coronary arteries
Throboangitis obliterans, also known as Buerger's disease, notice neutrophils and micro-abcesses

-foot claudication

-Raynaud's synderome: paroxysmal digital color change, ulceration and gangreen
What clinical findings present with this disease?
Throboangitis obliterans, also known as Buerger's disease

remitting, relapsing inflammation disorder that often leads to thrombosis of med sized vessels

-Tibial and radial arteries
How does this patient develop the above findings?
Abdominal atherosclerotic aneuysm

->pt presents with left flank pain, hypotension, and pulsating mass in abdomin

->transmural wall damage is expected
What 3 clinical findings would this pt present with?

What degree of wall damage is expected?
Microscopic polyangiitis

-small vessel vasuclitis

-see palpable pupura, glomerulonephritis p-ANCA antibodies 80% of time
This pt presents with what key clinical and lab findings?
vasa vasorum of aorta resulting in dilatation/aneurysm of arota and aortic ring

-ischemic destruction of elsastic tissue and muscel of media which results in scaring "tree-bark" appearance

->sacular aneurysm

->develop aortic valve regurg, see wide pulse pressure, difference btwn systolic and diastolic pressure, manifested by hyperdynamic circulation - pulstatig uvula, bounding pulses
What is the target of this disease which presents as a "tree bark" appreance?
Aortic dissection

1. tear of intima due to htn or underlying structural weakness in media, usually occur 10 cm of aortic valve

-Cystic medial degeneration (CMD), associated with ct disorders, elastic tissue is fragmented

2. pt presents with loss of pulse on left and severe retrosternal chest pain NOT radiating down arm, x-ray shows double barrel aorta
1. What pathologic change has occured here?

2. How does a pt in this condition present?
aortic dissection seen in young pt with Marfan syndrome, fibrillin syn mutation, or Ehler-Danlos syndrome, collagen defect mutation
what disorders are associated with this histological presentation?
Aortic dissection

1. tear of intima due to htn or underlying structural weakness in media, usually occur 10 cm of aortic valve

-Cystic medial degeneration (CMD), associated with ct disorders, elastic tissue is fragmented
What pathogenisis is associated with this?
These ar contraction band necrosis, hyper eosinophilc transvers bands in myocytes reflect hypercontraction of myofibrils following exposure to oxygen and circulating plasma Ca, the effects of reperfussion
What is the cause of this pathology?
What is this?

-no necrosis

-transient period of severe ischemia (ex: MI)

-function returns over time (days)

-flow/fxn mismatch
myocardial stunning
WHat is this?

-no necrosis

-chronic high grade stenosis (long standing)

-fxn returns immediately upon reflow

-flow/fxn matched
myocardial hypernation, see with severe CAD due to atherlosclerosis, cell fxn return if relieve high grade stenosis
What is this?

-intermittent occlusion

-good collateral fxn

-low hr

-low bp
best case for MI
What is this?

-abrupts total occlustion

-poor collateral fxn

-high hr

-high bp
worst case for MI
timing of histologic damage in MI?

very early; wavy fiber change, edema, hemorrhage; beginning neutrophilic infiltrate
4 to 12 hr after mi
timing of histologic damage in MI?

-heavey pmn inflitration
24 to 72hr after mi
timing of histologic damage in MI?

-macrophage appear
4 to 7 days after MI
timing of histologic damage in MI?

well-developed necrotic changes; prominent fibrovascular reaction in margins (early collagen deposition; pigment-laden macrophages)
10 days after MI
pump failure

-low co despite high filling pressure

-hypotension

-hypoperfusion: periphearl vasoconstriction, oliguria, altered mental status
What complication occured due to MI?
rv infaction

-occurs in 20% of inferior wall MI

-sign of RV failure: inc JVP, hypotension
MI complication?
Papillary muscle rupture

-inferior wall infarct can result in post medial papillary wall rupture

-also can be due to anteriolateral muscle rupture due to anterolateral wall infaction
MI complication?
ventricular aneurysm

-due to weakening of vent wall following large transmural infarct

-closely related to post-infarct vent expansion or remodeling
complicatin of MI?
What is this?

acute dilation and thinning of infact zone not explained by additional necrosis

-associated with higher mortality and higher incidence of heart failure, aneurysms, and rupture

-augments wall stress, impairs contractile fxn
infarct expansion, complication of MI
What is this?

new necrosis in same anatomical zone of orgnial MI
Infarct extension, complication of MI
rupture of free wall of infarcted ventricle occuring up to 5% of pt dying in hospital due to acute MI

-more common in htn pt

-occur btween 3 to 5 days after MI

-more common to occure in anterior or lateral lv

Clinical sign: cardiac tamponade and sudden death

-can involve septum and papillary muscles
MI complication?
pericarditis

-very common with trasmural MI

-result in pericardial frictional rub (leathery rub)

-can be acute -> 2 to 4 days after MI

-can be late, autoimmune response -> 2 to 10 wk after MI = Dressler's Synderome or post-MI synderome
MI complication?
-fever

-chest pain

-pericardial freictiona rub (leathery rub)

-elevated ESR

-elevated WBC

-chest pain relieved when sit up or forward
how does this pt present acutely?
Pt presents with past hx of cancer comes in bc fatigue, dyspnea, dizziness, sycope. Upon measuring bp, pt bp drops 12 mm Hg during inspiration. What is the cardiac conditon seen in this pt?
cardiac tamponade with paradoxical pulse
Pt with past exposure to radiation come in to see you because if fatigue and increase swelling in pt abdomin and legs. You notice that the pt distention of neck veins with inspiration and a loud early S3 sound. What cardiac disease does this pt present with?
chronic constrictive pericarditis seen in post malignancy with radiation

Kussmal' signs = distension of neck veins with inspiration

Pericardial knock = loud early S3 sounds
What organism is associated with acute endocarditis?
staph aureus - infection with high virulence organisms

-may infect normal valves

-destruction due to hyaluronidase production
What organism is associated with subacute endocarditis?
infection with low virulence organisms ex: strep viridans

-damage occurs to damaged or abnormal valves
What organism common with prosthetic valve infective endocarditis?
staph epidermidis
what do these 3 relate to?

1. rupture of leaflet, chordae tendinae, or papillary muscles

2. ring abcess, extension of infection to surrounding tissue

3. embolization or septic infact
complications of acute endocarditis
What type of prostetic cardiac valve could develop complications of mechcanical deterioation
bioprostetic cardiac valve from animals
leaflet perforation, due to acute endocarditis
complication for infective endocarditis
abcess

-ring abcess-> extension of infection to surrounding tissue
complication of infective endocarditis
pericarditis
complication of bacterial endocarditis?
1. Non-bacterial thromboitc endocarditis (NBTE)

2. malignancies, paticularly adenocarcinomas

3. deposition of small masses of fibrin, platelets and other blood components on leaflets but no micro-organisms and no valvular damaged needed/required
1. disease state?

2. common etiology?

3. definition?
gross exam:
-groups of small nodules along the line of valve closure (recall RF)

-aortic valve more commonly involved

Microscopically:
-nodules composed of fibrin and platelet

-underlying valve normal (no fibrosis or necrosis)
What is the pathology of this disease?
What prosthetic cardic valve can have the complication of hemolysis?
mechnical or man-made cardiac valves
bioprosthetic valve with paravalvular leak
what type of valve and valve complication can be seen here?
suppurative pericarditis

-pericardial space invaded by infective organism, organization is usually outcome not resolution
What are causes of this type of pericarditis?
fibrinous / serofibrinous

-most frequent, due to acute mi, dressler, uremia, radiation, RF, SLE, trauma, post surgical
type of pericarditis?
post surgical (adhesive) pericarditis

-type of chronic pericarditis due to surgery, TB, suppurative pericarditis and irradiation
type of pericarditis?
constrictive pericarditis

-type of chronic pericarditis

-hemodynamically resembles restrictive cardiomyopathy

-due to chronic inflammation and fibrosis/thickening which results in decreased ventricular compliance
type of pericarditis?
TB pericarditis

-chronic pericarditis, specifically, adhesive mediastinopericarditis
type of pericarditis?
type of pericardial effusion?

caused by congestive heart failure, hypoalbunemia of any cause
serous
type of pericardial effusion?

blunt chest trauma, malignancy
serosanguinous
type of pericardial effusion?

mediastinal lymphatic obstruction
chylous mediastinal lymphatic obstruction
etiology of primary myocarditis
viral: picorna virus, esp coxsackie A and B, others: ECHO, influenza, CMV, HIV
type of cardiomyopathy?

characterized by progressive cardiac hypertrophy, dilation and systolic dysfxn
dilated cardiomyopathy
myocarditis - mononuclear inflitrate with necrosis

actue, fulminating infection - lymphocytic infiltrates, myofiber degeneration in patchy, focal fashion
cardiac disease?
dialated cardiomyopathy - non specifica microscopic features including mixture of myocyte hypertrophy, interstitial fibrosis, and myocyte atrophy
cardiac disease?
hypertrophic cardiomyopathy - mutation in gene coding for heavy chain of B-myosin on chr 14

-leading cause of sudden death in young athletes
genetic mutation seen in 50% of familial cases for this disease
what cardiac disease is assocaited with adriamycin and has a globoid outline?
dialated cardiomyopathy
category of myocarditis:

chagas disease, toxoplasmosis, trichinosis
parasite
category of myocarditis:

lyme disease (borrelia), diptheria (endotoxin)
bacterial
category of myocarditis:

allograft rejection, SLE, drug hypersensitivity, and sarcodosis
Immune
category of myocarditis:

sarcoidosis, giant cell myocarditis
unknown
all of the following cause what cardic disease?

adriamycin (dose related > 500 mg/m2)

cyclophosphaminde

lithium

tricyclics

chloroquine
drug-induced cardiomyopathy
this is restrictive cardiomyopathy caused by hemochromoatosis

other causes include: amyliodosis, radiation injury, glycogen storage disease (pompe's disease)
What is the cause of this disease?
this is restrictive cardiomyopathy caused by hemochromoatosis

other causes include: amyliodosis, radiation injury, glycogen storage disease (pompe's disease)
What is the cause of this disease?
What cardiac disease has the following as primary causes:

1. endomyocardial fibrosis (primary form)children, young adults in Africa
• starts in apex and moves toward valves

2. Loeffler endomyocarditis
(eosinophilia)

3.endocardial fibroelastosis- children usually with congenital defect/aortic
valve
restrictive cardiomyopathy
restrictive cardiomyopathy, specifically due to hemochromotosis using Perl's iron stain
type of cardiac disease?
congenital cardiac disease?

1.due to rubella

2. pink on top and blue on bottom

3. hear machinery murmur

4. close giving indomethacin
patent ductus arteriosus
cardiac disease that presents histologically with ashoff bodies
myocarditis due to rheumatic fever
most common cause of congenital heart disease in children charcterized by defect in interventicular septum

-possibley developing eisenmenger syndrome leading to pul htn and cynosis from r to l shunt
VSD - ventricular septal defect
congenital defect seen in downs syndrome and fetal alcohol syndrome
ASD
associated with:

1. VSD

2. pulmonary stenosis

3. RVH

4. overriding aorta
tetralogy of fallot
most common cyanotic congenital heart disease
tetralogy of fallot
type of coarctation seen in children and associated with tuner's synderome
preductal coarctation of aorta
disease?

1. see disparity btwn upper and lower extermites pulse

2. associated with notching of ribs

3. inc risk of intracranial anerysm rupture
postductal coarcation of aorta
What disease is associated with cynotic spells and pt squattto improve symptoms?
Tetrology of Fallot, pt squatt to inc total systemic vascular resistance so to inc arterial pressure
What disease is associated with the following sx:

-splinter hemmorhages in nail bed

-glomerulonephritis

-roth spots

-jainway lesons

-osler node
infective endocarditis which causes mitral regurg
what is oxygen supply due to?
coronary perfusion pressure and coronary vascular resistance
what disease are children with vsd likely to develop?
pul htn due to eisenmenger synderome which causes the left to right shunt to change to right to left causing pul htn to develop and cynosis
coronary blood flow is based on?
myocardial consumption of O2
type of angina?

coronary artery vasospasm at rest with stress test showing ST elevation = transmural ischemia
prinzmetal angina
What coronary artery thrombosis is associated with mural thrombus?
LAD
triad for cardiac tamponade
1. sob with hypotension

2. elevated jvp

3. muffled heart sound
-pericarditis (fibrinous pericarditis)

-arthritis of large joints, subcutaneous nodules, erythema marginatum, myocarditis, pulmonary involvement (pleuritis; uncommon)
What was the likely cause of the friction rub when your patient was 12 years old? What other clinical manifestations may have been present?
-tests: echo, blood cultures

-slide shows acute bacterial endocarditis; therapy is IV antibiotics to treat impending sepsis
(heart valves are avascular and therefore difficult to eradicate the offending organism)
When your patient’s sister presented, what laboratory tests would be the most helpful in establishing the correct diagnosis? Based upon your diagnosis what therapy is indicated and why?
-tests: echo, blood cultures

-slide shows acute bacterial endocarditis; therapy is IV antibiotics to treat impending sepsis
(heart valves are avascular and therefore difficult to eradicate the offending organism)
When your patient’s sister presented, what laboratory tests would be the most helpful in establishing the correct diagnosis? Based upon your diagnosis what therapy is indicated and why?
-a.) sepsis secondary to acute bacterial endocarditis

-b.) acute mitral regurgitation secondary to ruptured papillary muscle and/or chordae tendineae
-arrhythmia

-c.) sepsis (flushed skin, hypotension)
What complications of acute endocarditis might have accounted for the patient’s demise? What pathologic findings would be associated with these complications? Which was most likely in our patient and why?
coagulation necrosis and liquefactive necrosis (septic infarction)
Describe in detail the histologic findings in the slides. What kinds of necrosis are present?
What are potential complication of a new mitral valve?
-at increased risk for endocarditis/paravalvular leaks (prosthetic valve)
-at risk for thrombosis (prosthetic valve)

-at risk for arrhythmias (atrial hypertrophy)

-other complications of prosthetic valves (i.e. mechanical deterioration, hemolysis)
-pericarditis (fibrinous pericarditis)

-arthritis of large joints, subcutaneous nodules, erythema marginatum, myocarditis, pulmonary involvement (pleuritis; uncommon)
What was the likely cause of the friction rub when your patient was 12 years old? What other clinical manifestations may have been present?
What complications of MI’s at this stage (5 days) might have accounted for the patient’s demise? What pathologic findings would be associated with these complications?
cardiogenic shock- >40% of LV infarcted and pulmonary edema
acute mitral regurgitation- ruptured papillary muscle and pulmonary edema
ruptured MI- pericardial sac filled with blood (tamponade)
arrhythmia- no changes or +/- pulmonary edema
The tissue section was taken from the posterior wall of the left ventricle. In which coronary artery would you expect to find a thrombus? What if the section were from the lateral or anterior ventricular wall?
LAD---anterior LV and anterior 2/3 of the interventricular septum
LCA---lateral wall of the LV (posterior wall in 10-20% of patients)
RCA---posterior wall of the LV and posterior 1/3 of the interventricular septum
reductions greater than 75% can cause critical stenosis resulting in ischemia on (manifest as angina pectoris)
In examining the heart at autopsy, you find atherosclerotic plaques in the left anterior descending and left circumflex coronary artery. The luminal diameter of the LAD is reduced by 90%. How is this finding significant?
drug of choice to treat stage 1 htn (145 - 159 / 90 - 99)
1st - hctz, chlorothalidone

2nd - ACEI, ARB, BB, CCB or combo
drug class?

inhibit active exchange of Cl-Na in distal convoluted tubule
thiazides
drug class?

inhibit reabsorption of Na in dital convoluted and collecting tubule
potasium sparing diuretics

-triamterne

-amiloride
drug class?

inhibit exchange of Cl-Na-K in the thick segment of acending loop of henle
Loop diuretics

-furosemide

-torsemide
drug of choice to treat stage 2 htn (> 160 / > 100)
2 drug combo, usually hctz and ACEI or ARB or BB or CCB
major ae: hypokalemia, hypotension, DM, gout

->dec morbidity and mortality
hctz
compelling indication for dieurtics
hf, high cad risk, dm, recurrent stoke prevention
drug group used to tx chf and htn

ae: acute renal failure (imp) and hypokalemia and hypomag
loop diuretics
ae: ototoxicity
loop diuretics
drug used when creatine clearance low
dont use hctz

use loop diuretics
drug group added to hctz and loop diuretics to tx hypokalemia
K sparing diuretics - triamterene, amiloride
what effect does salt sub like Mrs Dash have on drug txmt of htn
can cause hyperkalemia if pt on hctz or loop diuretic and K sparing diuretic
drug group which acts to inc hr, dec cardiac contractility, dec cond vel and ince refractory period of av node
bb
ae: bradycardia, bronchospasm, mask hypoglycemia in dm
bb
drug group?

contraindication: asthma

caution: pt with bradycardia due to lv failure
bb
ae: othostatic hypotension, syncope, hypotension
a-blockers: terazosin, prazosin, doxazosin
used to be used for bph
a-blockers: terazosin, prazosin, doxazosin
cardiac effects of ACEI
dec preload, dec afterload, inc co, inc sv, dec cardiac and venous remodeling
drug class?

ae: hyperkalemia, acute renal failure, cough (accum of bradykinin) and angioedema
ACEI: lisinopril, captropril, ramipril
compelling indication:
hf, post mi, cad high risk, dm, dec repeat stock
ACEI: lisinopril, captropril, ramipril
caution use in bilateral renal artery stenosis
ACEI: lisinopril, captropril, ramipril

ARB: valsartan, losartan, candesartan, irbesartan
used when pt develops cough due to ACEI
ARB: valsartan, losartan, candesartan, irbesartan
moa: blockade of aldosterone receptor
aldoserone antagonist: spironolactone, eplerenone
drug class with compelling indication for post mi and hf
aldoserone antagonist: spironolactone, eplerenone
moa: act on rate-limiting step in renin-angiotensin-aldosterone system
renin inhibitor: aliskiren
moa: block L-type calcium channel in cardiac cells and smooth muscle cells
ccb: dihydropyridines=> amlodipine and nifedipine

non-dihydropyridines=> diltiazem and verapamil
ccb which only vasodilate
dihydropyridines=> amlodipine and nifedipine
ccb which vasodilate and dec hr
non-dihydropyridines=> diltiazem and verapamil
what drug class has these compelling indication:
dm and cad high risk
ccb
What ccb have ae: bradycardia?
non-dihydropyridines=> diltiazem and verapamil
ae: peripheral edema and reflex tachycardia
dihydropyridines=> amlodipine and nifedipine
used to tx supraventricular tachycardia
non-dihydropyridines=> diltiazem and verapamil
vasodilator with ae of constipation
non-dihydropyridines> verapamil
cheep vasodilator which must be tapered off otherwise will cause htn crisis
clonidine
vasodilator dosed 3 or 4 times a day and causes rash and SLE-like rxn
hydralazine
inhibit platelet aggregation, prevent acute coronary syndrome
asa and clopidogrel
reduce O2 demand on heart, prevent sx of cardiac ischemia
bb, ccb
drug classes which reduce plaque formation, stabilzed plaque, dec long term risk :

-reduce cv risk
ACEI, ARB, eplerenone
gold standard tx for cad and dm
asa
tx for stable angina
bb (1st), ccb, nitro
tx for unstable angina
iv nitro, asa, bbl, anticoag

revascularize
how long in advance does asa or clopidogrel need to be stoped before surgery
5 - 7 days
drug which dec hr, dec contractility, dec O2 demand, dec ischemia
bb
added on to bb in tx of stable angina
ccb
order of drug add on for tx of angina
bb 1st, ccb 2nd, nitrates 3rd
long acting nitrate
isosorbid mononitrate
moa: alters the trans-cellular late Na current, alter Na-dependent Ca channel during myocardial ischemia

reserved for refractory pt

prolongs QT interval
ranolazine
ae: rhadomyolysis and lft elevation
statins
drug classes that dec mortality
hctz, bb, asa, acei, arb, spirolactone
drug classes that can cause acute renal failure
k-sparing, ACEI, aldosterone antagoinst
drug classes that cause hyperkalemia
K-sparking dieurtics, ACEI, renin inhibitor
how to tx htn crisis due to clonidine
intially tx with clonidine then taper pt off
T or F

You can change pt stage in HF but not class.
F, class based on sx, stage based on progression of disease state, sx (class) can be improved but disease state can not be reversed
AE: hypokalemia, angioedema, dry cough, renal insuffiency, hypotension
ACEI: lisinopril, captopril, enalapril, ramipril
what lab monitered when tx pt with ACEI
serum Cr
what pt characteristic will lend them to develop acute renal failure with ACEI?
dont use with pt in low volume state seen in pt with pul cong and pitting edema, also hf and bilateral renal stenosis leading to dec GFR
what is the lab value to moniter with dierutics in chf
fluids, i/o, electrolytes, weight
moa: antagonized aldosterone effect of facilitating myocardial fibrosis
spirolactone
ae of diuretic = gyneomastia

what drug to switch to?
spirolactone

eplerenone
ae: bradycardia, av block, arrythymia, confusion, visual disturbances, hyperkalemia in acute OD, n/v, diarrhea, narrow theraputic window
digoxin
moa: block Na-K ATPase
digoxine
early sign of digoxin toxicity
cns and gi toxicity
T or F

Digoxin can be pushed to treat a fib
F
cause venous vasodilation
nitrates
cause arterial vasodilation
hydralazine
ae: cyanide and thiocynate toxity
nitroprusside
T or F

htn pt and chf pt can take same doses of bb
F, with chf must start bb very lowest does and very gradually inc dose
moa: synthetic analog of brain natiuretic peptide
nesiritide
B agonist used in pt with acute decompensatd heart failure - stage III or IV, last resort
dobutamine
inhibit breakdown of cAMP

AE:hypotension, arrythmia, tachycardia
milrinone
used by IV for txmt in htn crisis
nitroprusside
ae of nesiritide
hypotension
asymtomatic chf pt with lv dysfxn, ef< 40%

txmt?
ACEI, ARBS
symptomatic chf pt, nyha II

txmt?
dieurtics and bb
symptomatic chf pt, nyha III

txmt?
inc diuretics, maybe add spirolactone or digoxin
symptomatic chf pt, nyha IV

txmt?
inotropes, vasodilator, specialzed therapy, transplant
vasodilators
hydralazine, nitrates
pressors
dopamine,ne, epi
dose of dopamine?

renal, cerebral and mesenteric vessel dilation
low dose
dose of dopamine?

mainly see B1 simulating effects, inc contractility and HR
med dose
dose of dopamine?

overwelming effect on A1 stimulation, inc SVR, inc afterload, inc bp
high dose
pressor indication
systolic bp < 90 mm Hg
-w/o hypovolemia
-frequently in spetic or cardiogenic shock
precaution with pressors
inc hr = arrhythmogenesis

inc O2 demand on heart

monitore for signs and sx of mycardial ischemia
tx hf and afib
amiodarone and dofetilide
ekg changes seen couple hours after MI
st elevation and inverted t wave
what changes in ekg are seen couple days after mi
normal st segment and normal t wave
when does the following histological change occur after MI?

continuing coagulation necrosis; pyknosis of nuclei, shrunken eosinophilic cytoplasm, neutrophilic infiltrate well developed
18-24 hours
when does the following histological change occur after MI?

scarring complete
> 4 weeks
when does the following histological change occur after MI?

beginning disintegration of dead myofibers and resorption of sarcoplasm; onset of marginal fibrovascular response (fibroblasts, macrophages)
3 - 7 days